Vanessa A. Fitsanakis, Ph.D.
About
Vanessa A. Fitsanakis, Ph.D. is a toxicologist whose research and professional work centers on neurotoxicology, pesticide toxicity, and the mechanisms by which environmental exposures affect the nervous system. Her published work examines how pesticides and fungicides, including glyphosate-containing herbicides and manganese/zinc ethylene-bis-dithiocarbamate compounds, disrupt mitochondrial function and generate reactive oxygen species, with much of this work conducted using the model organism Caenorhabditis elegans. She has also published on forensic alcohol calculations, including methodology for assessing uncertainty in those calculations using percentile ranges.
Her peer-reviewed publications appear in journals including the Journal of Forensic Sciences, Acta Neuropathologica, Toxicological Sciences, Environmental Toxicology and Pharmacology, and Neurotoxicology and Teratology, and her body of work spans more than 30 publications. She has contributed to toxicology education at the undergraduate level, including work aligned with the Society of Toxicology's efforts to develop learning frameworks for toxicology curricula.
Her forensic work includes matters involving pesticide neurotoxicity and alcohol-related calculations, areas directly supported by her published research. She holds a Ph.D. and maintains licensure consistent with her practice in toxicology.
Publications
- Assessing uncertainty in forensic alcohol calculations: The case for using percentile ranges.
- Neurotoxicity of pesticides.
- Society of Toxicology Develops Learning Framework for Undergraduate Toxicology Courses Following the Vision and Change Core Concepts Model.
- Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
- Transport of a manganese/zinc ethylene-bis-dithiocarbamate fungicide may involve pre-synaptic dopaminergic transporters.
- Chronic exposure to a glyphosate-containing pesticide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans.
- Acute exposure to a Mn/Zn ethylene-bis-dithiocarbamate fungicide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans.
- Caenorhabditis elegans chronically exposed to a Mn/Zn ethylene-bis-dithiocarbamate fungicide show mitochondrial Complex I inhibition and increased reactive oxygen species.
- Exposure of C. elegans eggs to a glyphosate-containing herbicide leads to abnormal neuronal morphology.
- The Toxicology Education Summit: building the future of toxicology through education.
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